Degenerative mitral valve disease, usually related to a severe form of mitral valve prolapse, is responsible for most cases of mitral regurgitation, which affects more than 3 million people in the United States. The disease can affect heart function, cause the heart to enlarge and ultimately lead to heart failure and death.

“Moderate or severe mitral regurgitation is the most frequent form of valvular disease in the United States and is often seen in older people. An estimated 2.5 million people were affected in 2000, a number expected to double by 2030 due to the aging population,” says UAB cardiologist Louis A. Dell’Italia, M.D., associate chief of staff for research at the Birmingham Veterans Affairs Medical Center. “However, we also see patients in their 30s and 40s with it. If we can manage this disease early with medications, we can prevent damage to the heart muscle so that when a patient does need surgery to repair or replace the mitral valve, the recovery can go better because their heart is in better shape.”

Beta-blockers are best known for their use in treating hypertension and cardiac arrhythmias and for use immediately following a heart attack to protect the heart muscle from more damage by diminishing the effects of adrenaline and other stress hormones.

The UAB research team published findings seven years ago demonstrating that using beta-blockers in animal models also diminished adrenaline in the hearts of animals with mitral regurgitation and prevented muscle damage. The current study sought to test those findings in humans with mitral regurgitation.

Degenerative mitral valve disease, usually related to a severe form of mitral valve prolapse, is responsible for most cases of mitral regurgitation, which affects more than 3 million people in the United States.

“We know from previous research that biological changes in the heart occur in patients with degenerative mitral valve disease well before we can see structural changes through standard cardiac imaging with echo, MRI or CT scans,” Dell’Italia says. “We do not know if the cause of the disease within the valve itself is due to a genetic defect or is a response to the wear and tear on the valve itself. We do know that blocking the adrenaline in animal models significantly improved heart muscle function.”

The research team looked at 38 asymptomatic patients with moderate-to-severe mitral regurgitation. Half were randomized to a placebo, and half received a beta-blocker. Magnetic resonance imaging of each patient’s heart was performed at the beginning of the study and at six-month intervals for two years. Progression of a patient’s mitral valve disease was judged on heart function and size at those six-month intervals.

“Everything we saw in these patients was exactly what we saw in the animal models,” Dell’Italia says. “The beta-blockers significantly improved heart function during a two-year follow-up in the human patients also. These findings provide empirical support for using beta-blockers in patients with chronic degenerative mitral regurgitation. The next step is a large multi-center clinical trial to confirm these effects on a larger patient population.”

Lead author Mustafa Ahmed, M.D., of the UAB Division of Cardiovascular Disease, says the team also plans to look at using beta-blockers in patients with mild mitral regurgitation to see if treating patients earlier can prevent progression even more.

“Treating people early is almost a preventive concept,” Ahmed says. “But we believe we have shown through this research physicians can keep patients from needing surgery longer using a drug that in the end also protects the heart muscle and makes for a better surgical outcome.”